Our research program has two main components. Firstly, to develop and test models of cognitive processes via study of the way these processes breakdown following brain injury or disease. Secondly, to evaluate the cognitive status of psychiatric patients in order to test hypotheses concerning possible neuroanatomic correlates of these disorders. Our studies of patients with Alzheimer's disease have addressed the question of whether object naming and other word-finding problems are due to a loss of knowledge versus impaired retrieval. We have obtained evidence in support of a model that posits that posterior temporal lobe pathology results in a degradation of semantic representations of objects. These degraded representations are, in turn, proposed to be responsible for impaired naming and other types of word-finding problems in patients with Alzheimer's disease. Our studies of psychiatric patients have indicated subtle psychomotor and cognitive slowing, impaired motor skill learning and other deficits consistent with involvement of subcortical regions in a subgroup of subjects in the relatively early stages of Human Immunodeficiency Virus infection. Moreover, progressive slowing of reaction time was documented over repeated testing sessions and was found to be highly correlated with increases of the concentration of a potent neurotoxin, quinolinic acid, in cerebral spinal fluid. In contrast, adults with Obsessive Compulsive Disorders performed normally on similar tasks suggesting that the types of deficits seen in patients with basal ganglia lesions as a result of Huntington's disease may provide a good model for HIV-related cognitive dysfunction, but not for adult OCD.